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HATs off to Hop: recruitment of a class I histone deacetylase incriminates a novel transcriptional pathway that opposes cardiac hypertrophy

机译:跃升为跃点:募集I类组蛋白脱乙酰基酶可阻止与心脏肥大相对应的新型转录途径

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摘要

Histone acetylation, regulated by two antagonistic enzymes — histone acetyltransferases (HATs) and histone deacetylases (HDACs) — results in transcriptional changes and also plays a critical role in cardiac development and disease. A new study shows that overexpression of the atypical transcriptional corepressor homeodomain-only protein (Hop) causes cardiac hypertrophy via recruitment of a class I HDAC. In contrast to the body of work on transcriptional mechanisms that drive cardiac hypertrophy, including class II HDACs, this report elucidates a novel growth-suppressing transcriptional pathway in cardiac muscle that opposes hypertrophic growth.
机译:组蛋白乙酰化受两种拮抗酶-组蛋白乙酰转移酶(HATs)和组蛋白脱乙酰酶(HDACs)的调节-导致转录变化,并且在心脏发育和疾病中也起着关键作用。一项新研究表明,非典型转录共加压因子仅同源异域域蛋白(Hop)的过表达通过募集I类HDAC导致心脏肥大。与驱动心脏肥大的转录机制(包括II类HDAC)的研究工作形成鲜明对比的是,该报告阐明了与肥大性生长相反的新型抑制心肌生长的转录途径。

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